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. 2022 Apr 25;11(5):832. doi: 10.3390/antiox11050832

Figure 3.

Figure 3

Inhibition of A2E accumulation by BCE in ARPE-19 cells. (A) ARPE-19 cells pretreated with BCE (10–50 μg/mL) or lutein (15 μg/mL) were treated with A2E-BDP (10 μM) for 24 h. The relative A2E level was quantified by measuring their fluorescence at 485 nm (excitation) and 535 nm (emission) using a fluorescence microplate reader. The results are presented as the mean ± standard deviation of two independent experiments (n = 2). ** p < 0.01, *** p < 0.001 vs. A2E-BDP. (B) Heatmap generated from RT-qPCR results performed on the in vitro RPE damage model. After 24 h of BL exposure, the total RNA was isolated using TRIzol reagent. cDNA synthesized from mRNA was used for RT-qPCR. The mRNA levels were normalized to 18S rRNA levels. Values represent the log2 fold-change relative to CTR. C, control; A, A2E; B, blue light; AB, A2E + BL. ATF3, activating transcription factor 3; CXCL8, C-X-C motif chemokine ligand 8; DUSP5, dual specificity phosphatase 5; HSPA5, heat shock protein family A (Hsp70) member 5; IL1B, interleukin 1 beta; PHLDA1, pleckstrin homology like domain family A member 1; PPARG, peroxisome proliferator activated receptor gamma; TRIB1, tribbles pseudokinase 1; TRIB3, tribbles pseudokinase 3.